NAP: Recovery (2014)
Cochran AJ, Little JP, Tarnopolsky MA, Gibala MJ. Carbohydrate feeding during recovery alters the skeletal muscle metabolic response to repeated sessions of high-intensity interval exercise in humans. J Appl Physiol. 2010; 108: 628-636.PubMed ID: 20056852
To examine the effect of manipulating CHO intake during recovery on the acute metabolic response to high-intensity interval exercise, including signaling cascades linked to mitochondrial biogenesis
- Healthy men were recruited to participate in the study
- Subjects were habitually active two to three times per week but not specifically trained in any particular exercise modality.
Ten healthy men were recruited for the study.
- Randomized crossover trial of two treatments, each separated by at least one week
- Each trial consisted of a morning (AM) and afternoon (PM) training session (five four-minute cycling at approximately 90% to 95% of heart rate reserve) separated by three hours of recovery during which subjects ingested a high-CHO drink (HI-HI) or non-energetic placebo (HI-LO) before PM exercise.
- Subjects consumed either 1.2g CHO per kg body weight−1 per hour−1 (HI-HI condition) or a taste-matched, non-energetic placebo (HI-LO condition) for the first two hours of the three-hour recovery period. CHO (Carbohydrate Energy Formula; maltodextrin, isomaltulose, dextrose) and placebo beverages were provided by Gatorade (Chicago, IL), and were identical in taste and color.
- Subjects were provided with 500ml of the appropriate beverage each of the first two hours of recovery and instructed to consume it at regular intervals. Supplementary water was ingested ad libitum during the three-hour recovery each exercise trial day.
All data were analyzed using a two-factor repeated-measures ANOVA with significance set at P≤0.05. Significant interaction and main effects were further analyzed using a Tukey HSD post-hoc test.
Timing of Measurements
- PGC-1a protein content
- Cytochrome oxidase subunit IV (COXIV) mRNA content
- Peroxisome proliferator-activated receptor ? coactivator 1-a (PGC-1a) mRNA content
- Muscle signaling proteins [Phosphorylated p38 MAPK (p-p38 MAPK) and phosphorylated-AMPK (p-AMPK)]
- Muscle metabolites [Muscle ATP and phosphocreatine (PCR) concentrations]
- Serum insulin and non-esterified fatty acid (NEFA) concentrations
- Physical activity and nutritional controls.
Independent VariablesHigh-glycemic carbohydrate (CHO) (HI-HI) or a non-energetic (non-E), isovolumetric taste-matched placebo (PLA) (HI-LO) and high-intensity cycling interval exercise (HIE).
- Diet was monitored during the study via 24-hour diet logs
- Subjects were asked to refrain from caffeine for 12 hours and alcohol and physical activity for 24 hours prior to the experimental trials.
- Initial N: 10 healthy men
- Attrition (final N): 10
- Age: 21±1 years
- Other relevant demographics: VO2peak was 51.0±1.6ml per kg−1 per minute−1
- Anthropometrics: 180±2cm; 78±3kg
- Location: Ontario, Canada.
- Average power output during the 10 work intervals was 205±7W or 2.6W per kg
- The workload elicited 94±1% and 96±1% of peak heart rate during AM and PM exercise, respectively, which corresponded to 91±1% and 94±1% of HRR. There were no differences between treatments.
- Serum insulin concentration decreased to a similar extent during AM exercise in both conditions (main effect for time, P=0.05), while serum NEFA did not change significantly during AM exercise
- In response to the nutritional intervention applied during recovery, serum insulin concentration was higher before PM exercise in HI-HI vs. HI-LO (P<0.001)
- Serum NEFA concentration was lower before and after PM exercise in HI-HI compared with HI-LO (P<0.001)
- Blood lactate increased during both AM and PM exercise, but there were no differences between treatments, whereas blood glucose remained unchanged at all -time points
- Muscle glycogen content decreased by approximately 30% in both the AM and PM sessions (main effect for time, P<0.001)
- Nutritional manipulation during recovery from the AM session did not appear to markedly alter glycogen resynthesis, and there were no differences between treatments at rest or after PM exercise
- Muscle ATP was not altered by HIE in either the AM or PM exercise sessions. However, after PM exercise, a significant interaction effect was detected such that ATP content was lower in HI-LO compared with HI-HI (P=0.01)
- Muscle PCR was reduced during AM and PM exercise in both conditions (main effects for time; P<0.01), but the decrease was significantly greater in the HI-LO condition vs. HI-HI after PM exercise (P<0.01)
- Phosphorylated p38 MAPK (p-p38 MAPK) and phosphorylated-AMPK (p-AMPK) increased by approximately four-fold and approximately two-fold, respectively, during AM exercise, with no difference between conditions (main effects for time, P<0.01)
- After PM exercise, p-p38 MAPK was approximately 50% higher in HI-LO compared with HI-HI (P=0.004). Changes in p-AMPK during PM exercise appeared similar to p-p38 MAPK, with HI-LO tending to be greater than HI-HI, but the difference was not statistically significant (P=0.19).
- Phosphorylated ACC (p-ACC) was increased after exercise in both AM and PM, but there was no difference between conditions (main effect for time, P<0.001)
- -GC-1a mRNA was unchanged immediately after exercise in AM but increased approximately eight-fold before PM exercise, with no difference between conditions (main effect for time, P<0.001)
- COXIV mRNA increased 3 h after the AM exercise with no difference between treatments (main effect for time, P = 0.05).
- There was no further increase in PGC-1a mRNA immediately after PM exercise while COXIV was not significantly different from baseline after PM exercise
- There was no effect of exercise or nutritional manipulation on whole muscle PGC-1a protein content.
- CHO ingestion, and not necessarily changes in muscle glycogen content per se, alters the metabolic response to repeated sessions of high-intensity interval exercise, and particularly the activation of p38 MAPK
- Nutritional manipulation of the p38 MAPK response to exercise is one potential mechanism to explain the enhanced muscle oxidative capacity and performance reported after training with CHO restriction
- A single 30-minute session of high-intensity interval exercise activates signaling pathways linked to mitochondrial biogenesis and in particular induced increases in PGC-1a and COXIV mRNA after three hours of recovery.
|Government:||Natural Sciences and Engineering Research Council of Canada (NSERC)|
- Earlier reports suggest that p38 MAPK activity is necessary for myogenic cell differentiation and plays an important role in glucose metabolism and energy expenditure. p38 MAPK can directly stimulate upstream transcription factors. However, there has been no direct evidence that p38 activity stimulates gene transcription in skeletal muscle, and it is not known whether activation of this pathway is sufficient to induce, and necessary for, skeletal muscle adaptation.
- In this study, the data suggest evidence of p38 MAPK could be involved in the altered skeletal muscle adaptive response after exercise training under conditions of restricted CHO intake
- Further studies are encouraged to see in large population and in different ethnic origin.
Quality Criteria Checklist: Primary Research
|1.||Would implementing the studied intervention or procedure (if found successful) result in improved outcomes for the patients/clients/population group? (Not Applicable for some epidemiological studies)||Yes|
|2.||Did the authors study an outcome (dependent variable) or topic that the patients/clients/population group would care about?||Yes|
|3.||Is the focus of the intervention or procedure (independent variable) or topic of study a common issue of concern to dieteticspractice?||Yes|
|4.||Is the intervention or procedure feasible? (NA for some epidemiological studies)||N/A|
|1.||Was the research question clearly stated?||Yes|
|1.1.||Was (were) the specific intervention(s) or procedure(s) [independent variable(s)] identified?||Yes|
|1.2.||Was (were) the outcome(s) [dependent variable(s)] clearly indicated?||Yes|
|1.3.||Were the target population and setting specified?||Yes|
|2.||Was the selection of study subjects/patients free from bias?||Yes|
|2.1.||Were inclusion/exclusion criteria specified (e.g., risk, point in disease progression, diagnostic or prognosis criteria), and with sufficient detail and without omitting criteria critical to the study?||Yes|
|2.2.||Were criteria applied equally to all study groups?||N/A|
|2.3.||Were health, demographics, and other characteristics of subjects described?||Yes|
|2.4.||Were the subjects/patients a representative sample of the relevant population?||???|
|3.||Were study groups comparable?||Yes|
|3.1.||Was the method of assigning subjects/patients to groups described and unbiased? (Method of randomization identified if RCT)||Yes|
|3.2.||Were distribution of disease status, prognostic factors, and other factors (e.g., demographics) similar across study groups at baseline?||N/A|
|3.3.||Were concurrent controls or comparisons used? (Concurrent preferred over historical control or comparison groups.)||N/A|
|3.4.||If cohort study or cross-sectional study, were groups comparable on important confounding factors and/or were preexisting differences accounted for by using appropriate adjustments in statistical analysis?||N/A|
|3.5.||If case control study, were potential confounding factors comparable for cases and controls? (If case series or trial with subjects serving as own control, this criterion is not applicable.)||N/A|
|3.6.||If diagnostic test, was there an independent blind comparison with an appropriate reference standard (e.g., "gold standard")?||N/A|
|4.||Was method of handling withdrawals described?||N/A|
|4.1.||Were follow-up methods described and the same for all groups?||Yes|
|4.2.||Was the number, characteristics of withdrawals (i.e., dropouts, lost to follow up, attrition rate) and/or response rate (cross-sectional studies) described for each group? (Follow up goal for a strong study is 80%.)||N/A|
|4.3.||Were all enrolled subjects/patients (in the original sample) accounted for?||Yes|
|4.4.||Were reasons for withdrawals similar across groups?||N/A|
|4.5.||If diagnostic test, was decision to perform reference test not dependent on results of test under study?||N/A|
|5.||Was blinding used to prevent introduction of bias?||Yes|
|5.1.||In intervention study, were subjects, clinicians/practitioners, and investigators blinded to treatment group, as appropriate?||Yes|
|5.2.||Were data collectors blinded for outcomes assessment? (If outcome is measured using an objective test, such as a lab value, this criterion is assumed to be met.)||N/A|
|5.3.||In cohort study or cross-sectional study, were measurements of outcomes and risk factors blinded?||N/A|
|5.4.||In case control study, was case definition explicit and case ascertainment not influenced by exposure status?||N/A|
|5.5.||In diagnostic study, were test results blinded to patient history and other test results?||N/A|
|6.||Were intervention/therapeutic regimens/exposure factor or procedure and any comparison(s) described in detail? Were interveningfactors described?||Yes|
|6.1.||In RCT or other intervention trial, were protocols described for all regimens studied?||Yes|
|6.2.||In observational study, were interventions, study settings, and clinicians/provider described?||N/A|
|6.3.||Was the intensity and duration of the intervention or exposure factor sufficient to produce a meaningful effect?||Yes|
|6.4.||Was the amount of exposure and, if relevant, subject/patient compliance measured?||N/A|
|6.5.||Were co-interventions (e.g., ancillary treatments, other therapies) described?||N/A|
|6.6.||Were extra or unplanned treatments described?||N/A|
|6.7.||Was the information for 6.4, 6.5, and 6.6 assessed the same way for all groups?||N/A|
|6.8.||In diagnostic study, were details of test administration and replication sufficient?||N/A|
|7.||Were outcomes clearly defined and the measurements valid and reliable?||Yes|
|7.1.||Were primary and secondary endpoints described and relevant to the question?||Yes|
|7.2.||Were nutrition measures appropriate to question and outcomes of concern?||Yes|
|7.3.||Was the period of follow-up long enough for important outcome(s) to occur?||Yes|
|7.4.||Were the observations and measurements based on standard, valid, and reliable data collection instruments/tests/procedures?||Yes|
|7.5.||Was the measurement of effect at an appropriate level of precision?||Yes|
|7.6.||Were other factors accounted for (measured) that could affect outcomes?||N/A|
|7.7.||Were the measurements conducted consistently across groups?||Yes|
|8.||Was the statistical analysis appropriate for the study design and type of outcome indicators?||Yes|
|8.1.||Were statistical analyses adequately described and the results reported appropriately?||Yes|
|8.2.||Were correct statistical tests used and assumptions of test not violated?||Yes|
|8.3.||Were statistics reported with levels of significance and/or confidence intervals?||Yes|
|8.4.||Was "intent to treat" analysis of outcomes done (and as appropriate, was there an analysis of outcomes for those maximally exposed or a dose-response analysis)?||N/A|
|8.5.||Were adequate adjustments made for effects of confounding factors that might have affected the outcomes (e.g., multivariate analyses)?||N/A|
|8.6.||Was clinical significance as well as statistical significance reported?||Yes|
|8.7.||If negative findings, was a power calculation reported to address type 2 error?||N/A|
|9.||Are conclusions supported by results with biases and limitations taken into consideration?||Yes|
|9.1.||Is there a discussion of findings?||Yes|
|9.2.||Are biases and study limitations identified and discussed?||Yes|
|10.||Is bias due to study's funding or sponsorship unlikely?||Yes|
|10.1.||Were sources of funding and investigators' affiliations described?||Yes|
|10.2.||Was the study free from apparent conflict of interest?||Yes|